Human IL-32 expression protects mice against a hypervirulent strain of Mycobacterium tuberculosis
2015; National Academy of Sciences; Volume: 112; Issue: 16 Linguagem: Inglês
10.1073/pnas.1424302112
ISSN1091-6490
AutoresXiyuan Bai, Shaobin Shang, Marcela Henao‐Tamayo, Randall J. Basaraba, Alida R. Ovrutsky, Jennifer L. Matsuda, Katsuyuki Takeda, Mallory M. Chan, Azzeddine Dakhama, William H. Kinney, Jessica Trostel, An Bai, Jennifer R. Honda, Rosane Duarte Achcar, John M. Hartney, Leo A. B. Joosten, Soohyun Kim, Ian M. Orme, Charles A. Dinarello, Diane Ordway, Edward D. Chan,
Tópico(s)Immune Response and Inflammation
ResumoSignificance Interleukin-32 (IL-32) is induced by IL-1β, Toll-like receptor agonists, and nucleotide oligomerization domain as well as by Mycobacterium tuberculosis ( MTB ). Expression of human IL-32γ in the lungs of mice reduced the burden of MTB in both the lungs but also in the spleen and was associated with increased survival. Mechanistically, increased numbers of host-protective innate and adaptive immune cells were present in the IL-32 transgenic mice. Alveolar macrophages from the transgenic mice were also better able to control MTB infection and had increased colocalization of MTB with lysosomes. IL-32 expression was increased in the surgically resected lungs of tuberculosis patients, particularly in macrophages, airway epithelial cells, B cells, and T cells. Thus, IL-32 enhances host immunity against MTB .
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